Diseases of the central nervous system remain among the most compelling maladies known to humankind. This is because neurological disorders are typically devastating to affected patients and their families, often robbing individuals of the qualities that we most strongly associate with being human, and because the vast majority of neurological and neurodegenerative disorders lack effective therapies. In the 1980s and 1990s, the advent of molecular genetics approaches to map and identify disease genes laid the foundation for a prodigious advance in our understanding of the pathogenic basis of numerous important neurological disorders.
Neuropathic pain (NP) is a complex condition that has been the subject of considerable basic and clinical research. As a result of this effort, considerable progress has been made in our understanding of the pathophysiology underlying NP. Mechanisms now thought to be involved in the development and maintenance of NP include alterations in peripheral nerves, dorsal root ganglia, and the spinal cord. These changes include upregulation and/or downregulation of neuropeptides and neurotransmitters and changes that occur at supraspinal sites and result in facilitation of pain transmission.
Neurodegenerative disorders are a heterogeneous group of diseases of the nervous system, including the brain, spinal cord, and peripheral nerves, that have many different aetiologies. Many are hereditary, some are secondary to toxic or metabolic processes, and others result from infections. Due to the prevalence, morbidity, and mortality of the neurodegenerative diseases, they represent significant medical, social, and financial burden on the society. Neuropathologically, these are characterised by abnormalities of relatively specific regions of the brain and specific populations of neurons. The degenerating neuron clusters in the different diseases determine the clinical phenotype of that particular illness.
Free radicals are highly reactive moieties playing an important role in health and disease. The central nervous system is especially vulnerable to free radical damage because of brain's high oxygen consumption, abundant lipid content and relative paucity of antioxidant enzymes compared with other tissues. Oxidative stress mediated cell damage in the pathophysiology of several CNS disorders has also been suggested. In view of the above, the present study was designed to investigate the effect of stress on neurobehavioral changes and the possible involvement of free radicals. Restraint stress (RS) was used as an experimental stressor and elevated plus maze was used as a test for anxiety.
Managing acute pathology of often relies on the addressing underlying pathology and symptoms of the disease. There is currently a need in the art for new compositions to treatment or delay of the onset of neurologic diseases and its associated complications progression.